gga-miR-2127 downregulates the translation of chicken p53 and attenuates chp53-mediated innate immune response against IBDV infection

Ouyang, Wei; Wang, Yongshan; Meng, Kai; Pan, Qunxing; Wang, Xiaoli; Xia, Xingxia; Zhu, Yu Cheng; Bi, Zhenwei; Zhang, Haibin; Luo, Kai

doi:10.1016/j.vetmic.2016.12.007

Cited by 27 publications

(23 citation statements)

References 36 publications

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“…Avian reovirus p17 protein regulates cell cycle and autophagy by activating the p53/PTEN pathway [ 21 ]. Infectious bursal disease virus infection increases the activity of chicken p53, which is targeted by gga-miR-2127 [ 22 ]. A recent study indicates CAV1-mediated endocytosis is advantageous for productive CSFV Shimen infection in macrophages [ 8 ].…”

Section: Discussionmentioning

confidence: 99%

Classical swine fever virus Shimen infection increases p53 signaling to promote cell cycle arrest in porcine alveolar macrophages

Ning

et al. 2017

Oncotarget

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Classical swine fever virus (CSFV) replicates in macrophages and causes persistent infection. Despite its role in disastrous economic losses in swine industries, the molecular mechanisms underlying its pathogenesis are poorly understood. The virus evades the neutralizing immune response, subverting the immune system to ensure its own survival and persistence. Our genome-wide analysis of porcine alveolar macrophage transcriptional responses to CSFV Shimen infection using the Solexa/Illumina digital gene expression system revealed that p53 pathway components and cell cycle molecules were differentially regulated during infection compared to controls. Further, we investigated the molecular changes in macrophages infected with CSFV Shimen, focusing on the genes involved in the p53 pathway. CSFV Shimen infection led to phosphorylation and accumulation of p53 in a time-dependent manner. Furthermore, CSFV Shimen infection upregulated cyclin-dependent kinase inhibitor 1A (p21) mRNA and protein. In addition, CSFV Shimen infection induced cell cycle arrest at the G1 phase, as well as downregulation of cyclin E1 and cyclin-dependent kinase 2 (CDK2). The expression of genes in the p53 pathway did not change significantly after p53 knockdown by pifithrin-α during CSFV Shimen infection. Our data suggest that CSFV Shimen infection increases expression of host p53 and p21, and inhibits expression of cyclin E1 and CDK2, leading to cell cycle arrest at the G1 phase. CSFV may utilize this strategy to subvert the innate immune response and proliferate in host cells.

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Section: Discussionmentioning

confidence: 99%

Classical swine fever virus Shimen infection increases p53 signaling to promote cell cycle arrest in porcine alveolar macrophages

Ning

et al. 2017

Oncotarget

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“…miR-142-5p was founded to decrease the activity of the IFN-β by directly by targeting the MDA5 and then promoting IBDV replication through IRF7 (interferon regulatory factor 7) signaling pathway [112]. Additionally, miR-2127 has been found to promote IBDV replication by suppressing p53 translation and attenuating p53-mediated innate immune response against IBDV infection [113].…”

Section: Mirnas Involved In Ibdmentioning

confidence: 99%

Epigenetic Regulation by Non-Coding RNAs in the Avian Immune System

Chen

Abdalla

et al. 2020

Life

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The identified non-coding RNAs (ncRNAs) include circular RNAs, long non-coding RNAs, microRNAs, ribosomal RNAs, small interfering RNAs, small nuclear RNAs, piwi-interacting RNAs, and transfer RNAs, etc. Among them, long non-coding RNAs, circular RNAs, and microRNAs are regulatory RNAs that have different functional mechanisms and were extensively participated in various biological processes. Numerous research studies have found that circular RNAs, long non-coding RNAs, and microRNAs played their important roles in avian immune system during the infection of parasites, virus, or bacterium. Here, we specifically review and expand this knowledge with current advances of circular RNAs, long non-coding RNAs, and microRNAs in the regulation of different avian diseases and discuss their functional mechanisms in response to avian diseases.

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“…In contrast, gga-miR-9* negatively regulated the host antiviral innate immune response by suppressing type I IFN production by targeting IRF2 (interferon regulatory factor 2), an important factor that functions in IFN antiviral signal transduction pathways, to promote IBDV replication (Table 1, Ouyang et al, 2015). gga-miR-2127 overexpression also promoted IBDV replication and could down-regulate the expression of antiviral innate immunity genes by targeting p53 (Table 1, Ouyang et al, 2017). Additionally, gga-miR-142-5p targeted chMDA5 (chicken melanoma differentiationassociated gene 5), which encodes a protein that recognizes RNA viral infections and initiates an antiviral innate immune response, to promote IBDV replication in an IRF7-dependent pathway (Table 1, Ouyang et al, 2018).…”

Section: Mirna and Infectious Bursal Diseasementioning

confidence: 99%

Research Progress on MicroRNAs Involved in the Regulation of Chicken Diseases

Wang

2020

J. Poult. Sci.

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MicroRNAs (miRNAs) are small, non-coding RNA molecules that inhibit protein translation from target mRNAs. Accumulating evidence suggests that miRNAs can regulate a broad range of biological pathways, including cell differentiation, apoptosis, and carcinogenesis. With the development of miRNAs, the investigation of miRNA functions has emerged as a hot research field. Due to the intensive farming in recent decades, chickens are easily influenced by various pathogen transmissions, and this has resulted in large economic losses. Recent reports have shown that miRNAs can play critical roles in the regulation of chicken diseases. Therefore, the aim of this review is to briefly discuss the current knowledge regarding the effects of miRNAs on chickens suffering from common viral diseases, mycoplasmosis, necrotic enteritis, and ovarian tumors. Additionally, the detailed targets of miRNAs and their possible functions are also summarized. This review intends to highlight the key role of miRNAs in regard to chickens and presents the possibility of improving chicken disease resistance through the regulation of miRNAs.

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gga-miR-2127 downregulates the translation of chicken p53 and attenuates chp53-mediated innate immune response against IBDV infection

Cited by 27 publications

References 36 publications

Classical swine fever virus Shimen infection increases p53 signaling to promote cell cycle arrest in porcine alveolar macrophages

Classical swine fever virus Shimen infection increases p53 signaling to promote cell cycle arrest in porcine alveolar macrophages

Epigenetic Regulation by Non-Coding RNAs in the Avian Immune System

Research Progress on MicroRNAs Involved in the Regulation of Chicken Diseases

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